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Neonatal Blood Gas Interpretation

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Author:    Patricia Hartley (RNC, MSN)


An adjunct to clinical assessment of respiratory disease is chemical assessment via blood gases. The purpose of obtaining blood gases in a neonate is to determine if the baby is adequately ventilating and/or perfusing. Blood gases are the basis for analyzing if oxygenation is adequate and for deducing what the acid base balance is in a particular neonate. The medical plan of care for the neonatal patient includes the frequency of blood gas determination, and it is every care provider’s responsibility to be cognizant of each blood gas sample drawn on the patient. The value of timely and accurate interpretation of blood gas results cannot be questioned. 

Technological advances, including artificial surfactant and high frequency ventilation, have increased the need for rapid response to changing clinical conditions. Equipment that will allow in-line blood gas monitoring with an indwelling probe is now available. It makes possible more frequent sampling without the concern of excessive blood loss, which is a major concern for the tiny neonates.



pH - The symbol used to measure the hydrogen ion (H+) concentration. As the H+ concentration increases, the pH decreases (acidosis); as the H+ decreases, the pH increases (alkalosis). A severely depressed pH indicates acute decompensation.

Acid-Base Balance - The pH is the result of the plasma bicarbonate/plasma carbonic acid relationship.

Acid - A substance which can donate H+; excess causes decreased pH (<7.25).

Base – A substance capable of accepting H+; a decrease of H+ causes increased pH (>7.45).

Lungs – Controls pH by varying the amount of CO2 that is excreted.

Kidneys – Control pH by varying the rate of excretion of HCO3-.

Acidosis – A physiologic state where a significant base deficit is present.

Metabolic Acidosis – Occurs when a disorder adds acid to the body or causes alkali to be lost faster than the buffer system (lungs or kidneys) can regulate the load.

Respiratory Acidosis – Occurs when carbon dioxide is not promptly vented by the lungs and carbon dioxide combines with bicarbonate to form carbonic acid.

Alkalosis – A physiologic state in which there is more than normal base present.

Metabolic Alkalosis – Occurs whenever acid is excessively lost or alkali is excessively retained. The acid-base ratio of the body is altered.

Respiratory Alkalosis – Occurs when carbon dioxide is excreted by the lungs in excess of its production rate by the body; the level of carbonic acid falls producing an excess amount of bicarbonate in relation to the acid content.

Compensation – The secondary physiologic process occurring in response to a primary disturbance in the acid-base balance by which the deviation of pH is lessened.

Correction – Is a change in the system originally affected by the primary disturbance by some intervention using available therapy.


Normal Values

The classification and interpretation of blood gases are based on a set of normal values. Values for the term and preterm infant differ slightly from values for the adult because of immaturity and the presence of fetal hemoglobin. In addition, the exact values accepted as normal may vary from institution to institution.

Normal Neonatal Arterial Blood Gas Values:

pH 7.35 - 7.45
PaCO2 35 - 45 mm Hg
PaO2 50 - 70 mm Hg (term infant)
45 - 65 mm Hg (preterm infant)
HCO3 22 - 26 mEq/liter
Base Excess -2 - + 2 mEq/liter
O2 saturation 92 - 94 %


Acceptable Blood Gas Values:

  < 28 weeks 38-49 wks Term infant with pulmonary hypertension Infant with BPD
PaO2 50 - 65 50 - 70 > 100 60 - 80
PaCO2 40 - 50 40 - 50 < 30 45 - 60
pH > 7.28 > 7.30 > 7.5 7.35 – 7.45
HCO3 18 - 24 20 - 24 > 24  > 20


Acid Base Balance

Acid-base balance is maintained within narrow limits by complex interactions between the respiratory system and the kidneys. There are four major components to the arterial blood gas: pH, PaCO2, bicarbonate (HCO3-) or base excess, and PaO2. Oxygen diffuses across the alveolar-capillary membrane, moved by the difference in oxygen pressure between the alveolus and the blood. In the blood, oxygen dissolves in the plasma and binds to hemoglobin. Arterial oxygen content (CaO2) is the sum of dissolved and hemoglobin bound oxygen as described by the following equation:

CaO2 = (1.37 x Hb x SaO2) + (0.003 x PaO2)


CaO2 = Arterial oxygen content (ml/100 ml of blood)
1.37 = Milliliters of oxygen bound to 1 g of hemoglobin at 100 percent saturation
Hb = Hemoglobin concentration (g/dl)
SaO2 = Percent of hemoglobin bound to oxygen (%)
0.03 = Solubility factor of oxygen in plasma (ml/mm Hg)
PaO2 = Oxygen partial pressure in arterial blood (mm Hg)

In the equation for arterial oxygen content, the first term (1.37 x Hb x SaO2) is the amount of oxygen bound to hemoglobin. The second term (0.003 x PaO2) is the amount of oxygen dissolved in plasma. Most of the oxygen in the blood is carried by hemoglobin. 

For example, if a premature has a PaO2 of 60 mm Hg, an SaO2 of 92 percent, and a hemoglobin concentration of 14 g/dl, CaO2 is the sum of oxygen bound to hemoglobin (1.37 x 14 x 92/100) = 17.6 ml, plus the oxygen dissolved in plasma (0.003 x 60) = 0.1 ml. In this example, only one percent of oxygen in blood is dissolved in plasma; 99 percent is carried by hemoglobin.

If the infant has an intraventricular hemorrhage and hemoglobin concentrations drops to 10.5 g/dl but PaO2 and SaO2remains the same, CaO2 equals 13.4 ml/dl of blood. Thus, without any change in PaO2 or SaO2 a 25 percent drop in hemoglobin concentration reduces the amount of oxygen in arterial blood by 24 percent. This concept is important to remember when taking care of patients with respiratory disease. These patients need to be monitored and, if low, corrected to keep an adequate level of oxygenation.

The force that loads hemoglobin with oxygen in the lungs and unloads it in the tissues is the difference in partial pressure of oxygen. In the lungs, alveolar oxygen partial pressure is higher than capillary oxygen partial pressure so that oxygen moves to the capillaries and binds to the hemoglobin. Tissue partial pressure of oxygen is lower than that of the blood, so oxygen moves from hemoglobin to the tissue. 

Several factors can affect the affinity of hemoglobin for oxygen. The relationship between partial pressure of oxygen and hemoglobin is referred to as the oxyhemoglobin dissociation curve. Alkalosis, hypothermia, hypocapnia, and decreased levels of 2, 3-diphosphoglycerate (2, 3 DPG) increase the affinity of hemoglobin for oxygen. Acidosis, hyperthermia, hypercapnia and increased 2, 3 DPG have the opposite effect, decreasing the affinity of hemoglobin for oxygen. This is referred to as hemoglobin dissociation curve shifting to the right.

This characteristic of hemoglobin facilitates oxygen loading in the lung and unloading in the tissue where the pH is lower and the PaCO2 is higher. Fetal hemoglobin, which has a higher affinity for oxygen than adult hemoglobin, is more fully oxygenated at lower PaO2 values. This high affinity is represented by a left shift on the curve of dissociation of hemoglobin.

Once loaded with oxygen, the blood should reach the tissues to transfer oxygen to the cells. Oxygen delivery to the tissue depends on cardiac output (CO) and arterial oxygen content (CaO2): Oxygen delivery = CO x CaO2.

The key concept is that when assessing a patient’s oxygenation, more information than just PaO2 and SaO2 should be considered. PaO2 and SaO2 may be normal, but if hemoglobin concentration is low or cardiac output is decreased, oxygen delivery to the tissue is decreased.

The pH scale is a mathematical expression of the acid-base balance of a solution. The number of hydrogen ions in a solution determines the acidity of that solution. An acid solution can donate hydrogen ions; a base solution can accept hydrogen ions. Blood pH is determined by the balance between acids, which results from the byproducts of metabolism, and the body’s buffer systems. For example, if the carbon dioxide is not excreted effectively by the lungs, it combines with water to form carbonic acid, which leads to an excess of hydrogen ions and the development of acidemia.

There are three major blood buffers to neutralize acid in order to maintain the acid-base balance. Of the three buffers (hemoglobin, serum protein, and bicarbonate) the bicarbonate system is predominant. Bicarbonate combines with hydrogen to form carbon dioxide and water, thereby buffering the acids and balancing the pH. If the carbon dioxide cannot be excreted by the lungs, the hydrogen ions can be returned to solution and result in acidemia.

H+ + HCO3  H2CO3   H2O = CO2

The lungs are primarily responsible for the carbon dioxide level (PaO2) and the kidneys control the plasma bicarbonate (HCO3-). Acting as an acid, carbon dioxide will add hydrogen ions; and bicarbonate acting as a base accepts ions. As the PaCO2 rises or HCO3- falls the pH will become more acidotic. As the CO2 falls or HCO3- rises the pH will become more alkalotic.

PaCO2 is directly related to respiratory status, pH abnormalities resulting from abnormal PaCO2 are considered respiratory in origin. Any abnormalities in HCO3- are considered metabolic in origin. Base excess (BE) reflects the concentration of buffer. Normal range is 0 +/- 2 mEq/liter of base. Positive values express an excess of base or a deficit of acid; negative values express a deficit of base or an excess of acid. When the base excess is negative, it is sometimes referred to as the base deficit. 

The body attempts to maintain a normal pH in two ways:

1.By correcting or altering the component responsible for the abnormality. For example if an increased level of carbon dioxide in the blood is causing respiratory acidosis, the body will attempt to increase excretion of carbon dioxide by the lungs and bring the causative factor, increased CO2, back to normal levels.
2.By compensating through alterations in the component that is not primarily responsible for the abnormality. Carbon dioxide and/or bicarbonate will be excreted or retained in order to balance the abnormal value. For example, if a high PaCO2 is causing respiratory acidosis, the body will attempt to excrete more acid and conserve HCO3- to compensate, although compensation by renal function is a slow mechanism and may take several days. If the PaCO2 is low, the body will rid itself of bicarbonate. The inverse is also seen. High HCO3- will be compensated by a high PaCO2; a low HCO3- will be compensated by a low PaCO2. Thus, subsequent abnormal values of carbon dioxide or bicarbonate may result from the compensation mechanism of the body attempting to bring the ratio of HCO3- to CO2 back to 20:1.

Critically ill neonates may be limited in their ability to compensate for problems. Respiratory disease limits the body’s ability to effectively lower PaCO2, and the neonatal kidney may be ineffective in conserving bicarbonate.

The terms applied to acid-base disorders can be a source of confusion. Alkalemia and acidemia refer to measurements of blood pH; acidosis and alkalosis refer to the underlying pathologic process. A blood pH less than 7.35 is said to be acidemic; a pH greater than 7.45 is alkalemic. The partial pressure of carbon dioxide and bicarbonate levels determine, respectively, the respiratory and metabolic contributions to the acid-base equation. For each disorder, compensatory mechanisms are indicated. Correction occurs where possible by addressing the underlying problem.

Respiratory acidosis results from the formation of excess carbonic acid because of increased carbon dioxide.

Blood gas findings: low pH, high PCO2, normal bicarbonate.

CNS depression – maternal narcotics during labor, asphyxia, severe intracranial bleeding, neuromuscular disorder, CNS dysmaturity (apnea or prematurity)Decreased Ventilation-Perfusion ratio
Obstructed airways, meconium aspiration, choanal atresia, bloody mucus, blocked endotracheal tube, external compression of airwayDecreased alveolar ventilation and decreased lung compliance
HMD, chronic pulmonary insufficiencyInjuries to thoracic cage
Diaphragmatic hernia, phrenic nerve paralysis and pneumothoraxIatrogenic (inadequate mechanical ventilation)

Compensation: over three to four days, the kidneys increase the rate of hydrogen ion secretion and bicarbonate re-absorption. Compensated respiratory acidosis is characterized by a low normal pH, with increased carbon dioxide and increased bicarbonate, caused by the retention of bicarbonate in the kidney to compensate for elevated carbon dioxide levels.

Respiratory alkalosis results from alveolar hyperventilation leading to a deficiency of carbonic acid.

Blood gas findings: high pH, low PCO2, and normal bicarbonate.

Iatrogenic (mechanical ventilation)
CNS irritation (pain)
Increase in alveolar ventilation

Compensation: the kidneys decrease hydrogen secretion by retaining chloride and excreting fewer acid salts. Bicarbonate re-absorption is also decreased. The pH will be high normal with low carbon dioxide and low bicarbonate levels.

Metabolic acidosis is a deficiency in the concentration of bicarbonate in the extracellular fluid. It is caused by any systemic disease that increases acid production or retention, or problems leading to excessive base losses. Examples are hypoxia leading to lactic acid production, renal disease, and loss of base because of diarrhea.

Blood gas findings: low pH, low bicarbonate, normal PCO2.

Decreased tissue perfusion
Sepsis, CHF
Renal failure
Renal tubular acidosis
Increase in lactic acid production

Increase in organic acids
Loss of base
Loss of base

Compensation: if healthy, the lungs will blow off additional carbon dioxide through hyperventilation. If renal disease is not a problem, the kidneys will respond by increasing the excretion of acid salts and the re-absorption of bicarbonate. The pH will be low normal with low levels of carbon dioxide and bicarbonate ions.

Metabolic alkalosis is an excess concentration of bicarbonate in the extracellular fluid. It is caused by problems leading to increased loss of acid.

Blood gas findings: high pH, high bicarbonate, normal PCO2.

Gastric suctioning
Severe vomiting
Diuretic therapy
Iatrogenic (gave too much HCO3)
Exchange transfusion
Loss of acid
Loss of acid
Loss of H+ ion via kidney
Adding a base
Citrate in anticoagulant is metabolized

Compensation: the lungs compensate by retaining carbon dioxide through hypoventilation. The pH will be high normal with high levels of carbon dioxide and bicarbonate ions.

Summary of Blood Gas Changes:

 Respiratory AcidosisMetabolic AcidosisRespiratory AlkalosisMetabolic Alkalosis
Base ExcessNormalDecreaseNormalIncrease


Blood Gas Sampling

Analysis of blood gases provides the clinician the basis for determining the adequacy of alveolar ventilation and perfusion. It is crucial that this test be collected and evaluated with an understanding of appropriate technique and potential sources of error.

Regardless of the type of sample obtained attention should be given to the following factors:

  Infection control or universal precautions. All types of blood gas sampling carry the risk of transmission of infection to the infant through the introduction of organisms into the blood stream. In addition, the risk of exposing the clinician to the infant’s blood makes it necessary to take appropriate precautions.
  Bleeding disorders. The potential for bruising and excessive bleeding should be evaluated, particularly if an arterial puncture is being considered.
  Steady state. Ideally, blood gases should measure the infant’s condition in a state of equilibrium. After changing ventilator settings or disturbing the infant, a period of 20 to 30 minutes should be allowed for arterial blood chemistry to reach a steady state. This period will vary from infant to infant.

Arterial Sampling

Arterial blood can be obtained either from an indwelling line or through intermittent sampling of a peripheral artery. The choice of sample site will depend on the clinical situation. An indwelling arterial catheter should be placed when it is anticipated that the neonate will require frequent arterial blood sampling. Several criteria are used to determine the need for an indwelling line. The criteria include gestational age, disease process, and the amount of oxygen required. Common sites for indwelling arterial lines are the umbilical, radial, posterior tibial, and dorsalis pedis arteries.
 Arterial blood can be obtained either from an indwelling line or through intermittent sampling of a peripheral artery. The choice of sample site will depend on the clinical situation. An indwelling arterial catheter should be placed when it is anticipated that the neonate will require frequent arterial blood sampling. Several criteria are used to determine the need for an indwelling line. The criteria include gestational age, disease process, and the amount of oxygen required. Common sites for indwelling arterial lines are the umbilical, radial, posterior tibial, and dorsalis pedis arteries.

Capillary Sampling

Capillary blood can be “arterialized” by warming the skin to increase local blood flow. Samples can be obtained from the outer aspects of the heel or from the side of a finger or toe. When perfusion is normal, it has been shown that capillary pH and PCO2 correlate well with arterial values. PO2 correlates if the partial pressure of oxygen in arterial blood is < 60, but not at higher levels.

Blood Gas Interpretation

Interpretation of blood gas data should follow a logical pattern. Initially evaluate the pH to determine if an acidemia or alkalemia is present. Then evaluate the respiratory parameter (PaCO2) and the metabolic parameter (HCO3-) to determine if the acidemia or alkalemia is respiratory or metabolic in origin. The clinical picture can become complex if abnormalities exist in both systems simultaneously. A review of the infant’s clinical statues, previous blood gas values, and treatment measures will help determine whether this is an ongoing compensation mechanism or two independent abnormalities. 

The arterial blood gas provides information about the pulmonary component of oxygenation, specifically the PaO2. Hypoxemia refers to a lower than normal arterial PO2, and hypoxia refers to inadequate oxygen supply to the body tissue. Preterm infants have a lower acceptable PaO2 values because HbgF results in increased oxygen delivery at lower PaO2

Hypoxemia results from lung disease or cyanotic congenital heart disease. Hypoxia may result from a number of factors, including heart failure, anemia, abnormal hemoglobin affinity for oxygen, and a decreased PaO2. The most common cause of hypoxemia is mismatching of ventilation and perfusion. It occurs when the amount of blood perfusing an alveolus or the amount of fresh gas entering the alveolus are not adequate for gas exchange. Normally in the lungs, some alveoli are better ventilated than others. Clinically significant mismatching results when decreased ventilation or perfusion interferes with the ability of the lung to provide adequate gas exchange. 

PaO2 of less than 45 to 50 mmHg is associated with vasoconstriction of pulmonary vasculature and vasodilation of the ductus arteriosus. Low PaO2s are implicated in the etiology of persistent pulmonary hypertension of the newborn (PPHN). 

Hyperoxemia (PaO2 > 100 mmHg) should also be avoided, especially in the preterm infant, where high levels of oxygen in the blood are associated with retinal injury. When interpreting neonatal PaO2s, it is important to identify whether the sample is pre- or post ductal in its origin because of the potential impact of shunting across the ductus resulting in lower PaO2 in post ductal samples.

Examples of Arterial Blood Gas Levels for Different Conditions:

Normal parameters

BE (base excess)-2

Respiratory Acidosis

BE (base excess)-4

Respiratory Alkalosis

BE (base excess)0

Metabolic Acidosis

BE (base excess)-10

Metabolic Alkalosis

BE (base excess)+8

The following steps can be used as a systematic way of evaluating parameters in neonatal blood gases:

1.Assess pH
2.Assess respiratory component
3.Assess metabolic component
4.Assess compensation status
5.Complete the acid-base classification
6.Formulate a plan

Acid-base imbalances are corrected where possible, through manipulation of the system that is causing the primary problem. This is done as follows:

Respiratory acidosis – assist in the removal of carbon dioxide through application of nasal continuous positive airway pressure (CPAP) or mechanical ventilation. For infants already on mechanical ventilation, removal of carbon dioxide can be facilitated by increasing the rate, peak inspiratory pressure (PIP), or positive end-expiratory pressure (PEEP). Sodium bicarbonate is usually not recommended for treating respiratory acidosis because it reacts with acids to form carbon dioxide

Respiratory alkalosis - for mechanically ventilated infants, reduce the rate or pressure on the ventilator.

Metabolic acidosis - where possible, treat the cause of the acidosis. If the acidosis is severe, sodium bicarbonate can be administered at a dose of 2 mEq/kg or according to the following formula:

Base deficit x (weight in kg) x (0.3)

The amount of bicarbonate calculated by this formula should theoretically correct half of the base deficit and should be administered slowly over 30 to 60 minutes. Fluid replacement may also be of benefit in treating metabolic acidosis because it helps the infant to metabolize lactic acid.

Metabolic alkalosis - treat the cause by removing acetate from IV fluids, by reducing diuretic doses, and by treating hyponatremia, hypokalemia, and hypochloremia.


Acid-base Imbalances, Compensation and Correction

Compensation occurs in response to a primary disturbance in acid-base equilibrium whereby the change in the pH is relieved. Compensation is a change in the system not originally affected by the primary disturbance. Correction is a change in the system originally affected by the primary disturbance, using available therapy by the clinician. 
Compensated respiratory acidosis is characterized by the retention of bicarbonate as a result of adjustment in renal function. The primary disturbance is the accumulation of carbon dioxide, thus increasing carbonic acid concentration. The kidneys respond to this disturbance by holding on to HCO3. This compensation by the kidneys can take several days if not corrected by ventilation therapy. When fully compensated the pH is near normal and PaCO2 values and HCO3 are increased.
Compensated metabolic acidosis is characterized by hyperventilation activated by the primary disturbance of an accumulation of acid that devours the available base. CO2 excreted through the lungs lowers the carbonic acid concentration to match the lower available bicarbonate. When fully compensated, the pH is near normal and the PaCO2and serum HCO3 values are both low.
Compensated respiratory alkalosis is characterized by the kidneys increasing their secretion of bicarbonate to restore the bicarbonate/carbonic acid ratio to normal. The primary disturbance is caused by hyperventilation and excessive elimination of CO2. When fully compensated, the pH is near normal, but PaCO2 and serum HCO3 are at the lower end of normal.
Compensated metabolic alkalosis is characterized by hypoventilation to diminish the elimination by CO2. The primary disturbance is the accumulation of bicarbonate by retaining CO2 the appropriate reaction between sodium bicarbonate and carbonic acid is restored. When compensated, the pH is almost normal but the PaCO2 and serum bicarbonate values are elevated.

Compensatory EffectCorrection
Metabolic Acidosis
pH < 7.35
Decreased PCO2Give bicarbonate and treat the cause
Respiratory Acidosis
pH < 7.35
Increased PCO2Increase HCO3Increase or assist ventilation
Metabolic Alkalosis
pH > 7.45
Increased HCO3Increased PCO2Give KCl 
Stop diuretics 
Treat cause
Respiratory Alkalosis
pH > 7.45
Decreased PCO2Decreased HCO3Attempt to stop hyperventilation

Correction of acidosis-alkalosis can be achieved sooner if one manipulates ventilator settings or gives bicarbonate to achieve a desired value. If you increase the pressure or rate on the ventilator CO2 will be blown off. If the rate or pressure is decreased CO2 will be retained. Severe metabolic acidosis should be treated with sodium bicarbonate 2 mEq/kg slow IV push. HCO3 should be diluted 1:1 with sterile H2O and ensure adequate ventilation. 

For acute correction of HCO3 base deficit: Base deficit X (wt in kg) X (0.3) Hypoxemia secondary to ventilator perfusion mismatching may be improved through the administration of supplemental oxygen. In addition, oxygenation can be improved by increasing the mean airway pressure in an infant receiving mechanical ventilation. See summary below:

Ventilator Corrections

Blood Gas ImbalanceVentilator Changes
Hypoxemia low PaO2Increase FiO2
Increase PEEP
Increase PIP
Hyperoxia high PaO2Decrease FiO2
Decrease PEEP
Hypercapnia high PaCO2Increase respiratory rate
Increase PIP (tidal volume)
Increase inspiratory time 
Increase flow rate
Decrease dead space
Hypocapnia low PaCO2Decrease respiratory rate
Decrease PIP
Decrease inspiratory time
Decrease flow rate
Increase dead space
Combination Disorders 
High PaCO2, low PaO2Increase inspiratory time
Increase PIP
High PaCO2, high or normal PaO2Decrease PEEP

Practice ABG Interpretation

1.Room Air
 pH = 7.22 mmHg PaCO2 = 61 mmHg PaO2 = 70 mmHg HCO3- = 24 mEq/l


The pH is lower than normal; therefore it would be labeled acidotic
        PaCO2 is higher than normal; therefore it would be labeled acidotic
        PaO2 is within normal range. Is the patient working to maintain the PaO2?
        HCO- is within normal range
        It is obvious the patient is suffering from acidosis. But is it respiratory or metabolic?
        Is it compensated or uncompensated?
        The HCO- is normal, therefore it is not metabolic, but respiratory.
        The ABG is uncompensated because the pH is not within normal range
        Uncompensated respiratory acidosis - consider CPAP
2.Mechanical ventilation rate 25, PIP 18, PEEP +4, FiO2 30% (33 week gestational age)
 pH = 7.49 mmHg PaCO2 = 26 mmHg PaO2 = 95 mmHg HCO3- = 22 mEq/l


The pH is high, indicating alkalemia.
        The PaCO2 is low, indicating a respiratory alkalosis.
        HCO- is normal.
        There is no compensation (pH is not normal).
        PaO2 is too high.
        Uncompensated respiratory alkalosis - consider reducing the rate or PIP and weaning oxygen.
3.Room Air infant with necrotizing enterocolitis on continuous gastric suction, TPN with sodium and potassium acetate. Capillary blood gas
 pH = 7.52 mmHg PCO2 = 41 mmHg PO2 = 55 mm Hg HCO3- = 35 mEq/l


The pH is high, indicating alkalemia.
        The PCO2 is high normal.
        The metabolic component is high, indicating a metabolic acidosis.
        There is no compensation (pH is not normal).
        The PO2 is adequate (capillary blood gas).
        Uncompensated metabolic alkalosis – consider eliminating the acetate and use chloride salts.
4.Premature infant receiving TPN (total parenteral nutrition) with adequate calories but the infant continues with weight loss. Capillary refill is sluggish and capillary gases:
 pH = 7.27 mmHg PCO2 = 36 mmHg PO2 = 57 mmHg HCO3- = 15 mEq/l


The pH is low indicating an acidosis.
        The PCO2 is normal.
        The metabolic component is low, indicating a metabolic problem.
        There is no compensation (pH is not normal).
        The PO2 is adequate (capillary blood gas).
        Uncompensated metabolic acidosis - consider giving volume to help metabolize lactic acid and adding acetates to lower metabolic acid load.
5.Premature infant on mechanical ventilation for respiratory distress (Rate 30, PIP 19, PEEP +5, and FiO2 40%). The infant has lost weight and has a serum sodium of 148 mEq/l.
 pH = 7.28 PaCO2 49 mmHg PaO2 = 56 mmHg HCO3- = 18 mEq/l


The pH is low, indicating an acidemia.
        The PaCO2 is high indicating respiratory acidosis.
        The metabolic component is low indicating a metabolic problem.
        There is no compensation (pH is not normal).
        The PaO2 is adequate.
        Uncompensated mixed respiratory and metabolic acidosis – increase ventilator rate. Consider giving volume to correct hypovolemia, which may be causing the metabolic acidosis.


Disorders of acid-base balance are diagnosed almost as frequently as blood gas sampling is undertaken in the neonatal population. Sick neonates have respiratory and metabolic systems that are in constant change in response to disease processes and also to therapeutic interventions. Quick responses to these changes will minimize the time an infant spends outside the desired range of blood pH and potential complications of treatments such as airway pressure (barotraumas) and oxygen. 

Arterial sampling allows for assessment of oxygenation, ability to remove carbon dioxide and acid-base status. Capillary blood samples are useful for evaluating CO2 removal and acid-base status but are not useful for evaluating oxygenation. It is important to approach blood gas interpretation systematically and to integrate physiology with the clinical history to provide optimal patient care and outcome. Monitoring a critically ill infant with a pulse oximeter will provide continuous information on his status by determining the pulse oxygen saturation. Intermittent assessment of the arterial blood gases will yield specific information on the acid-base balance.